Background
The prevalence of liver fibrosis has increased. It is defined as the reaction to the
chronic injury of the liver by which the hepatic parenchymal cell is distorted and
replaced by extracellular matrix.
Objective
To investigate the probable therapeutic properties of Carvedilol and Urolithin A on
liver fibrosis evedinced by thioacetamide (TAA) in rats.
Materials and methods
The study was conducted on 36 mature male albino rats which was distributed in
four groups (nine rats each): The control group, (TAA) group, which received 200
mg/kg of (TAA) by (Ip) injection three times a week, Urolithin A group, received both
(TAA) and urolithin A solution (50 mg/kg) by (Ip) injection every day, and Carvedilol
group, given (TAA) and carvedilol (10 mg/kg) orally. All treatments were given for
eight weeks. Serum concentrations of (AST), (ALT), and (ALP) were determined and
the histopathological and immunohistochemical staining were used to evaluate the
hepatic tissues.
Results and conclusion
TAA-treated rats showed pathological hepatic damage and substantial elevations in
serum liver enzymes and hepatic malondialdehyde (MDA) concentration.
Additionally, it reduced the activity of superoxide dismutase (SOD) and catalase
(CAT) in the liver tissue. When urolithin A or carvedilol were given in combination
with (TAA), they markedly diminished the (MDA) concentration in the liver tissues
and the serum liver enzymes while augmenting the activity of the liver tissue’s (SOD)
and (CAT). The histopathological and biochemical alterations prompted by (TAA)
administration were ameliorated under the influence of Urolithin A and Carvedilol.
Carvedilol exhibited a significantly superior hepatoprotective and anti-fibrotic effect
compared to Urolithin A. |
